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COMMONLYASSOCIATED CONDITIONS

Osteoarthritis (OA)

Knee pain due to OAis often associated with pes anserine bursitis, both of which may need specific treatment.

Higher grades of OAassociated with a thicker pes anserine bursa and larger area of bursitis (1)[C]

Valgus knee deformity

Obesity

Diabetes mellitus (questionable association)

DIAGNOSIS

HISTORY

Medial knee pain is the most common complaint.

Pain is located 4 to 6 cm distal to the medial joint line on the anteromedial aspect of the tibia.

Pain exacerbated by knee flexion:

–Going up or down stairs

–Getting out of a chair

PHYSICALEXAM

Common findings include:

–Tenderness to palpation at the pes anserine insertion

30% of asymptomatic patients will have tenderness to deep palpation in this area.

–Pain worsens with flexion of the knee against resistance.

–Localized swelling of the pes anserine insertion

Findings that suggest an alternative diagnosis: joint effusion, tenderness directly over the joint line, erythema or warmth, locking of the knee, systemic signs such as fever or pain with passive knee movement

DIFFERENTIALDIAGNOSIS

Medial collateral ligament injury

Medial meniscal injury

Medial plica syndrome

Medial compartment OA Semimembranosus bursitis

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Popliteal/meniscal cyst

Tibial stress fracture

Septic arthritis

DIAGNOSTIC TESTS & INTERPRETATION

Initial Tests (lab, imaging)

Primarily a clinical diagnosis

Lab work not indicated

Imaging is not indicated unless there is concern for bony injury/fracture, ligamentous injury, or meniscal tear.

Follow-Up Tests & Special Considerations

Ultrasound (US)

–Can demonstrate focal edema within the pes anserine bursa but has poor correlation with clinical findings

–Many patients with the clinical diagnosis of pes anserine bursitis have no morphologic changes of the pes anserine complex on US.

MRI: can demonstrate inflammation of the bursa and delineate the pes anserine bursa from other structures. T2-weighted axial images are best on MRI.

–No large studies have evaluated the correlation between the clinical diagnosis of pes anserine bursitis and radiographic evidence of pes anserine pathology on MRI.

–May see fluid in the pes bursa on MRI in 5% of asymptomatic patients

TREATMENT

Pes anserine bursitis is often self-limited. Conservative therapy is most common:

Relative rest and activity modification to avoid offending movements (especially knee flexion)

Ice to the affected area

Physical therapy for knee strengthening and range of motion activities (2)[C]

NSAIDs for pain control

Corticosteroid injection

Weight loss to improve biomechanical forces at the knee Extracorporeal shock wave therapy (3)[C]

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MEDICATION

First Line

NSAIDs, such as ibuprofen (800 mg PO TID) or naproxen (500 mg PO BID), are common first-line therapy.

Second Line

Corticosteroid injection combined with local anesthetic provides relief in many patients.

–Inject at the point of maximal tenderness using standard aseptic technique.

–~2 mL of anesthetic (i.e., 1% lidocaine) and 1 mLof steroid (i.e., 40 mg of methylprednisolone) is injected into the bursa using a small (e.g., 25-gauge, 1-inch) needle.

–Insert needle perpendicular to the skin until bone is felt and then withdraw slightly before injecting.

–Avoid injecting directly into the tendon (4)[C].

US-guided injection is superior to blind injection (5)[C].

Platelet-rich plasma injections also provide pain relief (6)[C].

ADDITIONALTHERAPIES

Hamstring and Achilles stretching

Quadriceps strengthening—particularly of the vastus medialis (terminal 30 degrees of knee extension)

Adductor strengthening

SURGERY/OTHER PROCEDURES

No role for surgery in routine isolated cases

Drainage or removal of bursa may be used in severe/refractory cases.

ONGOING CARE

Home exercise program focusing on flexibility and strengthening

DIET

Consider dietary changes as part of a comprehensive weight-loss program if obesity is a contributing factor.

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PROGNOSIS

Most cases of pes anserine syndrome respond to conservative therapy. Recurrence is common, and multiple treatments may be required.

REFERENCES

1.Uysal F, Akbal A, Gökmen F, et al. Prevalence of pes anserine bursitis in symptomatic osteoarthritis patients: an ultrasonographic prospective study. Clin Rheumatol. 2015;34(3):529–533.

2.Sarifakioglu B, Afsar SI, Yalbuzdag SA, et al. Comparison of the efficacy of physical therapy and corticosteroid injection in the treatment of pes anserine tendino-bursitis. J Phys Ther Sci. 2016;28(7):1993–1997.

3.Khosrawi S, Taheri P, Ketabi M. Investigating the effect of extracorporeal shock wave therapy on reducing chronic pain in patients with pes anserine bursitis: a randomized, clinical-controlled trial. Adv Biomed Res. 2017;6:70.

4.Stephens MB, Beutler AI, O’Connor FG. Musculoskeletal injections: a review of the evidence. Am Fam Physician. 2008;78(8):971–976.

5.Finnoff JT, Nutz DJ, Henning PT, et al. Accuracy of ultrasound-guided versus unguided pes anserinus bursa injections. PM R. 2010;2(8):732–739.

6.Rowicki K, Płomiński J, Bachta A. Evaluation of the effectiveness of platelet rich plasma in treatment of chronic pes anserinus pain syndrome. Ortop Traumatol Rehabil. 2014;16(3):307–318.

ADDITIONALREADING

Alvarez-Nemegyei J. Risk factors for pes anserinus tendinitis/bursitis syndrome: a case control study. J Clin Rheumatol. 2007;13(2):63–65.

Chatra PS. Bursae around the knee joints. Indian J Radiol Imaging. 2012;22(1):27–30.

Rennie WJ, Saifuddin A. Pes anserine bursitis: incidence in symptomatic knees and clinical presentation. Skeletal Radiol. 2005;34(7):395–398. Wittich CM, Ficalora RD, Mason TG, et al. Musculoskeletal injection. Mayo Clin Proc. 2009;84(9):831–836; quiz 837.

CODES

ICD10

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M70.50 Other bursitis of knee, unspecified knee

M70.51 Other bursitis of knee, right knee

M70.52 Other bursitis of knee, left knee

CLINICALPEARLS

Consider pes anserine syndrome in patients presenting with medial knee pain.

Pes anserine syndrome is relatively common in athletes and in older, obese patients with OA.

Tenderness over the insertion of the pes anserine tendon on the medial aspect of the tibia 4 to 6 cm distal to the joint line is common in asymptomatic patients as well—correlation of the entire clinical picture is necessary for accurate diagnosis.

Consider pes anserine syndrome in patients who have persistent symptoms associated with medial-sided OA.

Treatment is typically conservative. Alocal steroid/anesthetic injection may provide pain relief and enhance rehabilitation.

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CANDIDIASIS, MUCOCUTANEOUS

Sheila O. Stille, DMD Hugh Silk, MD, MPH, FAAFP

BASICS

DESCRIPTION

Heterogeneous mucocutaneous disorder caused by infection with common commensal Candida species

Characterized by superficial infection of the skin, mucous membranes, and nails

>20 Candida species cause infection in humans. Candida albicans is most common, at 80% of isolates.

Candidiasis affects:

–Aerodigestive system

Oropharyngeal candidiasis (thrush): mouth, pharynx (1)[A]

Angular cheilitis: corner of the mouth

Esophageal candidiasis

Gastritis and/or ulcers, associated with thrush; alimental or perianal

–Other systems

Candida vulvovaginitis: vaginal mucosa and/or vulvar skin

Candidal balanitis: glans of the penis

Candidal paronychia: nail bed or nail folds

Folliculitis

Interdigital candidiasis: webs of the digits

Candidal diaper dermatitis and intertrigo (within skin folds)

Synonym(s): monilia; thrush; yeast; intertrigo

ALERT

Vaginal antifungal creams and suppositories can weaken condoms and diaphragms.

Pregnancy Considerations

Vaginal candidiasis is common during pregnancy.

Topical treatment during pregnancy should be extended by several days (typically a full 7-day course).

Vaginal yeast infection at birth increases the risk of newborn thrush but is of

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no overall harm to baby.

EPIDEMIOLOGY

Common in the United States; particularly with immunodeficiency and/or uncontrolled diabetes

Age considerations

–Infants and seniors: thrush and cutaneous infections (infant diaper rash)

–Women of childbearing age: vaginitis

–Prepubertal or postmenopausal: yeast vaginitis

–Predominant sex: female > male

Incidence

Unknown—mucocutaneous candidiasis is common in immunocompetent patients. Complication rates are low.

Prevalence

Candida species are normal flora of oral cavity, pharynx, esophagus, and GI tract that are present in >70% of the U.S. population.

ETIOLOGYAND PATHOPHYSIOLOGY

C. albicans (responsible for 80–92% vulvovaginal and 70–80% oral isolates). Altered cell–mediated immunity against Candida species (either transient or chronic) increases susceptibility to infection (2)[A].

Genetics

Chronic mucocutaneous candidiasis is a heterogeneous, genetic syndrome with infection of skin, nails, hair, and mucous membranes; typically presents in infancy

RISK FACTORS

Immune suppression (antineoplastic treatments, transplant patients, cellular immune defects) (2)[A]

Malignant diseases

AIDS or hematologic/immune disorders (neutropenia)

Corticosteroid use

Smoking and alcoholism

Hyposalivation (Sjögren disease, drug-induced xerostomia, radiotherapy) (2) [A]

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Broad-spectrum antibiotic therapy

Douches, chemical irritants, and concurrent vaginitides alter vaginal pH and predispose patients to candidal vaginitis.

Denture wear, poor oral hygiene

Birth control pills, intrauterine devices

Endocrine alterations (DM, pregnancy, renal failure, hypothyroidism)

Uncircumcised men at higher risk for balanitis

GENERALPREVENTION

Use antibiotics and steroids judiciously; rinse mouth after inhaled steroid use (1)[A].

Avoid douching.

Treat other vaginal infections.

Minimize perineal moisture (wear cotton underwear; frequent diaper changes).

Clean dentures often; use well-fitting dentures and remove during sleep.

Optimize glycemic control in diabetics.

Preventive regimens during cancer treatments (2)[A]

Treat with HAART in HIV-infected patients.

Antifungal prophylaxis against oral candidiasis is not recommended in HIVinfected adults unless patients have frequent or severe recurrences (2)[A].

COMMONLYASSOCIATED CONDITIONS

HIV

Leukopenia

Diabetes mellitus

Cancer and other immunosuppressive conditions

DIAGNOSIS

HISTORY

Infants/children

–Oral: adherent white patches on oral mucosae or on the tongue that do not wipe away easily

–Perineal: erythematous rash with characteristic satellite lesions; painful if skin layer eroded. 40–75% of diaper rashes lasting >3 days are C. albicans (2)[A].

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– Angular cheilitis: painful fissures at corners of mouth

Adults

–Vulvovaginal lesions; whitish “curd-like” discharge; pruritus; burning

–Balanitis: erythema, erosions, scaling; dysuria

Immunocompromised hosts

–Oral: white, raised, painless, distinct patches; red, slightly raised patches

–Esophagitis: dysphagia, odynophagia, retrosternal pain; usually concomitant thrush

–GI symptoms: abdominal pain

–Folliculitis: follicular pustules

PHYSICALEXAM

Infants/children

–Oral: white, raised, distinct patches within the mouth; when wiped off, reveals red base

–Perineal: erythematous maculopapular rash with satellite pustules or papules

–Angular cheilitis: tender fissures in mouth corners, often cracked and

bleeding Adults

–Vulvovaginal: thick, whitish, cottage cheese–like discharge; vagina or perineum erythema

–Balanitis: erythema, linear erosions, scaling

–Interdigital: redness, excoriation at base and webspaces of fingers and/or

toes, possible maceration Immunocompromised hosts

–Oral: white, raised, nontender, distinct patches; red, slightly raised patches; thick, dark-brownish coating; deep fissures

–Esophagitis: Often, oral thrush is visible.

–Folliculitis: follicular pustules

–Interdigital: redness, excoriations at base of fingers and/or toes, often maceration

DIFFERENTIALDIAGNOSIS

For oral candidiasis

–Leukoplakia; lichen planus; geographic tongue

–Herpes simplex; erythema multiforme

–Pemphigus

Baby formula or breast milk can mimic thrush—easier to remove than thrush

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(no red base when wiped away)

Hairy leukoplakia: does not rub off; dorsum and lateral margins of tongue

Angular cheilitis from vitamin B or iron deficiency, staphylococcal infection, or edentulous overclosure

Bacterial vaginosis and Trichomonas vaginalis tend to have more odor, itch, and a different discharge.

DIAGNOSTIC TESTS & INTERPRETATION

Initial Tests (lab, imaging)

10% KOH slide preparation: mycelia (hyphae) or pseudomycelia (pseudohyphae) yeast forms; few WBC or 15–30% NaOH (3,4)[A]

Associated with normal vaginal pH (<4.5)

Barium swallow: cobblestone appearance, fistulas, or dilatation (denervation)

Diagnostic Procedures/Other

If first-line treatment fails, obtain samples for culture.

Sabouraud dextrose agar plates for fungal growth (3)[A]

Biopsy of hyperplastic candidiasis (3)[A]

Esophagitis may require endoscopy with biopsy (if suspicious for cancer).

HIV-seropositive patients with thrush and dysphagia relieved by antifungal have Candida esophagitis.

Test Interpretation

Biopsy: epithelial parakeratosis with polymorphonuclear leukocytes in superficial layers; periodic acid–Schiff staining reveals candidal hyphae (3,4) [A].

TREATMENT

GENERALMEASURES

Screen for immunodeficiency (diabetes, HIV).

MEDICATION

First Line

Vaginal (choose 1)

– Miconazole (Monistat) 2% cream: one applicator or 200 mg (one

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